Proliferative vitreoretinopathy (PVR) is a common cause of blindness in diabetics and those with penetrating eye injuries and is the major obstacle to successful retinal reattachment surgery. The clinical disorder in humans is marked by aggregation and nonneoplastic proliferation of cells on the inner or outer surfaces of the retina and on the vitreous. The cells are of varied origin, including retinal pigment epithelial cells, fibroblasts and glia. Recent advances made in the surgical and pharmacological treatment of PVR have not been adequate to successfully manage the disease in most patients. For this reason, research efforts must be directed toward a better understanding of the nature of the proliferative process so as to make possible new prophylactic and therapeutic approaches. The proposed work is designed to explore the hypothesis that fibroblast growth factor (FGF), a substance with is mitogenic for cells of various types, promotes the cellular proliferation that is the hallmark of PVR, following its local release from cells under conditions of retinal detachment, retinal detachment surgery, trauma or diabetes. Using the rabbit as an experimental model, it will be determined whether administration of the basic form of FGF (bFGF) to the intact vitreous stimulates the proliferation of cells endogenous to the posterior chamber, leading to the formation of cellular membranes and traction retinal detachment. Similarly, the effects of injecting bFGF intravitreally with a suspension of cultured cells (i.e. fibroblasts, retinal pigment epithelial cells or glia) at variable densities will be ascertained. Complementary experiments will determine whether intravitreally injected heparin neutralizes the mitogenic activity of bFGF when the latter is injected either alone or in conjunction with a cell suspension. Intraocular changes will be monitored postoperatively by indirect ophthalmoscopy and will be confirmed by histological examination of the tissues.